NR 507 Week 4 Midterm Study Guide (Variant 1&2)
Questions With Correct Answers 100% Verified
Mid Term Study Guide NR 507
Pulmonary
1. Concepts of anticholinergic drug and asthma:
Anticholinergic drugs: block acetylcholine binding (primarily in the lungs) -promotes
bronchiole dilation through decrease in the parasympathetic response (tiotropium &
ipratropium) is fast acting
2. Bronchitis & associated pathogenesis:
Begins with an exposure to an irritant (tobacco smoke) – activates bronchiole smooth
muscle constriction- mucus secretion- release of inflammatory mediators(histamine,
prostaglandins & leukotrienes) normal response to occasional airborne site irritants-
over bronchitis is over long term 3 months for over 2 consecutive years- = smooth
muscle hypertrophy = increase bronchoconstriction, hypertrophy and hyperplasia of
goblet cells= mucus hypersecretion, epithelia cell metaplasia = non-ciliated squamous
cells, migration of more WBCs to site = inflammation and fibrosis in bronchial wall,
thickening and rigidity of bronchial basement membrane= narrowing of bronchial
passageways : Increased mucus production- inflammation process = weight loss, loss
of appetite, muscle weakness (interleukin controls appetite) increases protease
activity= breakdown of elastin in the connective tissues of the lung= destruction of the
wall between the alveoli and lungs = large ineffective air sacs develop-elastic recoil of
bronchial wall -destroys bronchi and cant dilate and they stay constricted =air trapping :
Chronic bronchitis
=Dyspnea- air trapping increased mucus, increase WOB r/t chronic
bronchoconstriction Cough- irritated and inflamed bronchial epithelia membrane
Hypoxia & Hypercapnia -from impaired gas exchange
3. Chronic bronchitis and related acid/base disturbance:
Hypercapnia (CO2 retention) = Respiratory acidosis
r/t anatomical changes ventilation is compromised esp. exhalation = alveolar
hyperinflation) expanded thorax) hypercapnia CO2 retention = respiratory acidosis\
4. Perfusion:
the actual exchange of O2 and CO2 in the bloodstream occurs via the alveoli and
pulmonary capillaries: the passage of fluid to an organ or a tissue usually referring to
delivery of blood to an area
5. Blood flow between the heart and lungs in chronic bronchitis:
Poor ventilation leads to r to l shunting to occur= deoxygenated blood passes from r
ventricle to the lungs to the l ventricle without adequate perfusion (gas exchange) the
kidneys respond by secreting erythropoietin increasing RBC production the increase in
RBC increase O2 carrying capacity -the increase blood volume increases the workload
of the pulmonary and cardiovascular systems increasing blood volume and
vasoconstriction = pulmonary HTN= increase workload on the R ventricle =cardiac
hypertrophy= R side HF or Cor Pulmonale
6. Asthma signs and symptoms:
,NR 507 Week 4 Midterm Study Guide (Variant 1&2)
Questions With Correct Answers 100% Verified
Coughing esp. at night, chest tightness, shortness of breath, wheezing on exhalation, and
rapid breathing: Characteristics: airway inflammation, bronchial hyperactivity, smooth
muscle spasms, =
, NR 507 Week 4 Midterm Study Guide (Variant 1&2)
Questions With Correct Answers 100% Verified
excessive mucus production, hypertrophy of bronchial smooth muscle -obstruction and
decrease alveolar ventilation
7. Bronchioles in asthma:
There are 3 layers of the bronchiole which is a tube-like structure surrounding the lumen or
airway passageway: innermost layer is composed of columnar epithelial cells and goblet
cells-
The outermost layer is composed of smooth muscle cells responsible for the ability of the
airway to constrict and dilate – the middle layer is the laminar propria and it is embedded
with connective tissue and immune cells: in asthma these protective features go
overactive =inflammation response= damage to host tissue=hypertrophy of the
bronchioles smooth muscle and excessive mucus production: bronchioles spasm-mucus
production-obstruction
8. Alveolar hyperinflation with asthma:
Increase mucus production from the goblet cells in the inflammation process forms plugs of
mucus and pus and block alveolar passageways leading to air trapping and hyperinflation
= erosion of airway tissue
9. Polycythemia Vera:
a rare blood disease in which the body makes too many RBCs making the blood thicker
than normal causing blood clots; is often a result of chronic low levels of O2 in the blood,
the kidney compensates by increase secretion of erythropoetin, the primary hormone
responsible for stimulating RBC production= as a result patients with chronic bronchitis
will often exhibit increased HCT levels and can develop a condition called secondary
polycythemia vera.
10. Mechanism of action of anticholinergic drugs to treat asthma:
Anticholinergic drugs bind to muscarine receptors and block the action of acetylcholine
They reduce Broncho motor tone =bronchodilation: block acetylcholine binding,
bronchodilation, decrease parasympathetic response
Cardiovascular:
11. Review concepts of Cardiac Output:
Cardiac Output= Heart rate x Stroke volume\
Cardiac output: is the volume of blood ejected by each ventricle per minute
(75 bpm x 70ml = 5.25 L/min) 5 L of blood in the body= every drop of blood circulates the
body
-per heartbeat per minute
Cardiac output decrease with age at a rate of 1% per year after the age of 30 (other
factors can accelerate the rate of decline)
Cardiac output is a key component of HF and is important to understand the connection
b/t HR & SV:
DECRESE in HR (longer filling time) INCREASE in
SV INCREASE in HR (shorter fill time) DECREASE
in SV
Questions With Correct Answers 100% Verified
Mid Term Study Guide NR 507
Pulmonary
1. Concepts of anticholinergic drug and asthma:
Anticholinergic drugs: block acetylcholine binding (primarily in the lungs) -promotes
bronchiole dilation through decrease in the parasympathetic response (tiotropium &
ipratropium) is fast acting
2. Bronchitis & associated pathogenesis:
Begins with an exposure to an irritant (tobacco smoke) – activates bronchiole smooth
muscle constriction- mucus secretion- release of inflammatory mediators(histamine,
prostaglandins & leukotrienes) normal response to occasional airborne site irritants-
over bronchitis is over long term 3 months for over 2 consecutive years- = smooth
muscle hypertrophy = increase bronchoconstriction, hypertrophy and hyperplasia of
goblet cells= mucus hypersecretion, epithelia cell metaplasia = non-ciliated squamous
cells, migration of more WBCs to site = inflammation and fibrosis in bronchial wall,
thickening and rigidity of bronchial basement membrane= narrowing of bronchial
passageways : Increased mucus production- inflammation process = weight loss, loss
of appetite, muscle weakness (interleukin controls appetite) increases protease
activity= breakdown of elastin in the connective tissues of the lung= destruction of the
wall between the alveoli and lungs = large ineffective air sacs develop-elastic recoil of
bronchial wall -destroys bronchi and cant dilate and they stay constricted =air trapping :
Chronic bronchitis
=Dyspnea- air trapping increased mucus, increase WOB r/t chronic
bronchoconstriction Cough- irritated and inflamed bronchial epithelia membrane
Hypoxia & Hypercapnia -from impaired gas exchange
3. Chronic bronchitis and related acid/base disturbance:
Hypercapnia (CO2 retention) = Respiratory acidosis
r/t anatomical changes ventilation is compromised esp. exhalation = alveolar
hyperinflation) expanded thorax) hypercapnia CO2 retention = respiratory acidosis\
4. Perfusion:
the actual exchange of O2 and CO2 in the bloodstream occurs via the alveoli and
pulmonary capillaries: the passage of fluid to an organ or a tissue usually referring to
delivery of blood to an area
5. Blood flow between the heart and lungs in chronic bronchitis:
Poor ventilation leads to r to l shunting to occur= deoxygenated blood passes from r
ventricle to the lungs to the l ventricle without adequate perfusion (gas exchange) the
kidneys respond by secreting erythropoietin increasing RBC production the increase in
RBC increase O2 carrying capacity -the increase blood volume increases the workload
of the pulmonary and cardiovascular systems increasing blood volume and
vasoconstriction = pulmonary HTN= increase workload on the R ventricle =cardiac
hypertrophy= R side HF or Cor Pulmonale
6. Asthma signs and symptoms:
,NR 507 Week 4 Midterm Study Guide (Variant 1&2)
Questions With Correct Answers 100% Verified
Coughing esp. at night, chest tightness, shortness of breath, wheezing on exhalation, and
rapid breathing: Characteristics: airway inflammation, bronchial hyperactivity, smooth
muscle spasms, =
, NR 507 Week 4 Midterm Study Guide (Variant 1&2)
Questions With Correct Answers 100% Verified
excessive mucus production, hypertrophy of bronchial smooth muscle -obstruction and
decrease alveolar ventilation
7. Bronchioles in asthma:
There are 3 layers of the bronchiole which is a tube-like structure surrounding the lumen or
airway passageway: innermost layer is composed of columnar epithelial cells and goblet
cells-
The outermost layer is composed of smooth muscle cells responsible for the ability of the
airway to constrict and dilate – the middle layer is the laminar propria and it is embedded
with connective tissue and immune cells: in asthma these protective features go
overactive =inflammation response= damage to host tissue=hypertrophy of the
bronchioles smooth muscle and excessive mucus production: bronchioles spasm-mucus
production-obstruction
8. Alveolar hyperinflation with asthma:
Increase mucus production from the goblet cells in the inflammation process forms plugs of
mucus and pus and block alveolar passageways leading to air trapping and hyperinflation
= erosion of airway tissue
9. Polycythemia Vera:
a rare blood disease in which the body makes too many RBCs making the blood thicker
than normal causing blood clots; is often a result of chronic low levels of O2 in the blood,
the kidney compensates by increase secretion of erythropoetin, the primary hormone
responsible for stimulating RBC production= as a result patients with chronic bronchitis
will often exhibit increased HCT levels and can develop a condition called secondary
polycythemia vera.
10. Mechanism of action of anticholinergic drugs to treat asthma:
Anticholinergic drugs bind to muscarine receptors and block the action of acetylcholine
They reduce Broncho motor tone =bronchodilation: block acetylcholine binding,
bronchodilation, decrease parasympathetic response
Cardiovascular:
11. Review concepts of Cardiac Output:
Cardiac Output= Heart rate x Stroke volume\
Cardiac output: is the volume of blood ejected by each ventricle per minute
(75 bpm x 70ml = 5.25 L/min) 5 L of blood in the body= every drop of blood circulates the
body
-per heartbeat per minute
Cardiac output decrease with age at a rate of 1% per year after the age of 30 (other
factors can accelerate the rate of decline)
Cardiac output is a key component of HF and is important to understand the connection
b/t HR & SV:
DECRESE in HR (longer filling time) INCREASE in
SV INCREASE in HR (shorter fill time) DECREASE
in SV
